Vasoconstriction via voltage‐gated Ca 2+ Channels is impaired in the Femoral Principal Nutrient Artery of Aged Rats

Abstract

Age-related declines in skeletal blood flow may contribute to reduced bone mass and increased fracture risk. Previous reports linked impaired endothelium-dependent vasodilation of the femoral principal nutrient artery (PNA) with declines in femoral bone blood flow. However, enhanced vasoconstriction of the PNA with advancing age may also contribute to reduced skeletal perfusion. PURPOSE: We evaluated the vasoconstrictor properties of the PNA via voltage-gated Ca2+ channels and α-adrenergic stimulation. METHODS: PNAs from Fischer-344 young (4–6 mo) and aged (24–26 mo) rats were isolated and cannulated. Vasoconstriction to potassium chloride (KCl; 10–100 mM) and norepinephrine (NE: 10−9 – 10−4 M) was assessed. RESULTS: KCl-induced vasoconstriction was attenuated ~31% in aged vs. young rats. No differences in vasoconstriction occurred in the presence of NE, an α1- and α2-adrenoceptor agonist. DISCUSSION: Age-related declines in femoral bone blood flow may result from altered vasomotor properties of the femoral PNA (e.g., reduced vasodilator capacity, enhanced vasoconstrictor capacity, or both). Results from the present investigation indicate that vasoconstriction is not enhanced in the femoral PNA of aged rats. In fact, vasoconstriction via voltage-gated Ca2+ channels is impaired and no differences in α-adrenergic vasoconstriction occurred between young and aged rats. Therefore, age-related declines in femoral bone perfusion appear to result from attenuated endothelium-dependent vasodilation as opposed to enhanced vasoconstriction of bone resistance arteries. Supported by NASA grant NCC2-1166.